Cortical surface area and subcortical volume lower in individuals with bulimia nervosa compared with controls.
Researchers at the Icahn School of Medicine at Mount Sinai found that people with bulimia nervosa have structural differences in brain regions involved in reward and motivation, as well as social and sensory processing, and that more frequent binge eating is associated with more widespread differences in brain structure. Their findings were recently published in JAMA Psychiatry.
Bulimia nervosa is the second most common eating disorder in the world, characterized by recurrent binge eating and compensatory behaviors. Compared to other psychiatric illnesses, little is known about its neurobiology, and previous neuroimaging studies have generally included small numbers of participants and produced inconsistent findings.
“This study gives us the clearest evidence to date that bulimia nervosa is associated with reproducible differences in brain structure. We were surprised that the differences we identified in the brain’s outer layer involved a structural feature that is largely established early in development,” says Laura A. Berner, PhD, Director of the Center for Computational Psychiatry at Mount Sinai.
Laura A. Berner, PhD
Dr. Berner and colleagues from the global ENIGMA (Enhancing NeuroImaging Genetics through Meta-Analysis) consortium analyzed MRI brain scans from 369 females with bulimia nervosa and 417 females without an eating disorder across 17 international cohorts.
In comparison to people without an eating disorder, those with bulimia nervosa had lower volume of the nucleus accumbens – a brain region involved in processing reward and motivation. They also had lower surface area in regions of the temporal cortex – a brain area involved in sensory and social processing.
More frequent binge eating was associated with lower surface area in additional regions involved in cognitive control, reward value estimation, awareness of bodily signals, and processing and regulating emotions. In contrast, the frequency of compensatory behaviors—the measure currently used to define bulimia nervosa severity—was not associated with brain structure.
The findings suggest that specific symptoms, like binge eating, may have distinct neurobiological correlates. Because the study examined participants at a single point in time, longitudinal research is needed to determine whether these differences precede or follow illness onset.
“Our findings raise important questions about whether some of these brain differences could be markers of vulnerability to developing the illness. At the same time, the findings should not be interpreted to mean that the brain is fixed, or that a person’s outcome is predetermined,” says Dr. Berner. “We are excited about the next steps: understanding what these findings mean for the function of the affected brain circuits, and how these insights can ultimately help us identify better targets for prevention and treatment.”